Aging is a process that affects us all, unless you’re (un)lucky enough to die before the age of 25 from a freak yachting accident. Things start to break down after a while; replicating cells start to make mistakes in their DNA copies, your organs start to irreversibly scar, your collagen stops being elastic, and you start recognising yourself in the Biomedical Sciences module guide on the Biology of Aging. I’m only 22 (happy sodding birthday, me), and I’ve already got back pain and a general distrust of teenagers.
In short, getting old sucks, and hence people have tried to stop it. Treatments have usually focused on the symptoms of aging as opposed to the root cause, as the root cause has not even been remotely understood until now. But now it seems that the University of San Diego, California have come up with a potential explanation.
If you would like to read the full paper, it’s called Multigenerational silencing dynamics control cell aging, by Yang Li et al. And it’s free to access on PNAS, but be warned, the biochemistry gets very heavy, so here’s a short summary:
Aging revolves around something called chromatin. This is a complex of DNA and histones, the latter being a group of proteins that wrap the DNA around themselves like thread on a spool. A single histone spool is called a nucleosome, and the collective term for all these nucleosomes is chromatin. Then you wrap these spools around each other, and then wrap this super-thread around itself to form a single chromosome. With me so far?
Think of DNA as being computer code, while histones are the index
This is where it gets complicated. DNA has its own alphabet, using A, T, C, and G to spell out whatever protein you want in its own language. Histones also act as signals to various cellular enzymes to help them determine if the DNA they’re looking at is useful genes or just junk that’s just lying around. Think of DNA as being computer code, while histones are the index; instead of .jpg or .mp3, you have .protein, .tRNA, .virus, and so on.
While massively over-simplified, this is general the function of chromatin. Euchromatin is used to loosely wrap all the important stuff, while junk regions and viruses entrapped in our DNA are tightly bound up in heterochromatin so that they never see the light of day. Yes, you did read that right. We have viruses lodged in our DNA, but that’s a whole other story.
Anyway, this is where this newly discovered aging mechanism comes into play. Euchromatin is open to the nuclear environment, and as such is more likely to be hit by any DNA-damaging elements. That’s usually a bad sign, as this can cause mutations that will kill the cell, or even make it develop into a cancer. Heterochromatin is more closed up than euchromatin, so DNA wrapped up in it suffers far less damage.
What scientists discovered was that every now and then, their test cells would package up euchromatin-containing areas with heterochromatin to limit their exposure to DNA-damaging elements. Later on, these cells would de-package their heterochromatin back to euchromatin so that they could use the DNA that’s wrapped around it.
Now for the bad news: all this work was done on yeast, and therefore some of it translates poorly to human physiology. Take it from me when I say that this isn’t much of a big deal as yeast replication shares many core elements with human cell cycles. It just means that there’ll need to be a lot more work done before we can start thinking about slowing aging in humans using this process as a guide. Try comparing a painting to a photograph of the same thing; that’s the same level of difference we’re dealing with here.
Take antioxidants, avoid barbecues, and stop having fun
But like that one song by Still Remains, the worst is yet to come. Scientists also tried to completely stop this switching, and this caused the cells to die even more quickly than before, so that’s not really an option. If the DNA was in the euchromatin state, it would accumulate damage faster than usual and the yeast would die. If the DNA was wrapped in heterochromatin instead, the cell would die from not being able to produce the right proteins and RNAs. Either way, the switching was key.
The study concluded that in order to delay aging, we’d have to somehow enhance the switching capability of the cells. Some yeast cells lost the switching ability of their own volition, and these proceeded to eventually die, and it seems likely that our cells are doing the same thing. So while there isn’t a miracle cure yet, I can offer some advice; take antioxidants, don’t stay in the sun for too long, avoid barbecues, and generally stop having fun.
Last modified: 19th November 2017